{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"bioRxiv"}],"indexed":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T14:27:49Z","timestamp":1785421669607,"version":"3.56.0"},"posted":{"date-parts":[[2026,5,17]]},"group-title":"Physiology","reference-count":86,"publisher":"openRxiv","license":[{"start":{"date-parts":[[2026,5,17]],"date-time":"2026-05-17T00:00:00Z","timestamp":1778976000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"award":["R01HD071302"],"award-info":[{"award-number":["R01HD071302"]}],"id":[{"id":"https:\/\/ror.org\/01cwqze88","id-type":"ROR","asserted-by":"publisher"}]},{"award":["R01DC020889"],"award-info":[{"award-number":["R01DC020889"]}],"id":[{"id":"https:\/\/ror.org\/01cwqze88","id-type":"ROR","asserted-by":"publisher"}]},{"award":["T32HL007249"],"award-info":[{"award-number":["T32HL007249"]}],"id":[{"id":"https:\/\/ror.org\/01cwqze88","id-type":"ROR","asserted-by":"publisher"}]},{"DOI":"10.13039\/100008335","name":"Arizona Biomedical Research Commission","doi-asserted-by":"crossref","award":["RFGA 2023-008-29"],"award-info":[{"award-number":["RFGA 2023-008-29"]}],"id":[{"id":"10.13039\/100008335","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2026,5,17]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                <jats:p>\n                  Perinatal opioid exposure is a prevalent clinical concern linked to respiratory instability and adverse infant outcomes. The opioid buprenorphine is prescribed as a medication for opioid use disorder during pregnancy and used to treat neonatal opioid withdrawal syndrome, yet its direct effects on neonatal control of breathing have not been examined. Here, we asked how acute buprenorphine exposure affects breathing at rest, and during chemoreceptor stimulation. Using dual-chamber head-out plethysmography, we measured pulmonary ventilation rate (V\u0307\n                  <jats:sub>I<\/jats:sub>\n                  ) and metabolic rate in awake male and female Sprague-Dawley neonatal rats on postnatal days 4-5 (P4\u20135) during eupnea and a hypoxic-hypercapnic (HH) challenge. The effects of buprenorphine and two opioid receptor antagonists, naloxone hydrochloride, or peripherally restricted naloxone methiodide, were assessed using a repeated measures design. V\u0307\n                  <jats:sub>I<\/jats:sub>\n                  during eupnea and HH were markedly depressed following buprenorphine administration. Buprenorphine reduced V\u0307O\n                  <jats:sub>2<\/jats:sub>\n                  and V\u0307CO\n                  <jats:sub>2<\/jats:sub>\n                  and produced ventilatory equivalents for O\n                  <jats:sub>2<\/jats:sub>\n                  and CO\n                  <jats:sub>2<\/jats:sub>\n                  consistent with frank hypoventilation, driven by reduced breathing frequency and tidal volume (V\n                  <jats:sub>T<\/jats:sub>\n                  ). When administered after buprenorphine, neither naloxone hydrochloride nor naloxone methiodide could rescue the buprenorphine-mediated hypoventilation in eupnea or during HH. In contrast, pre-treatment with either naloxone hydrochloride or naloxone methiodide attenuated buprenorphine-induced hypoventilation by preserving V\n                  <jats:sub>T<\/jats:sub>\n                  . These findings demonstrate that neonatal protective chemoreceptor reflexes are depressed by buprenorphine and suggest that pre-treatment with a peripheral opioid receptor antagonist could mitigate buprenorphine-induced hypoventilation without inducing opioid withdrawal.\n                <\/jats:p>\n                <jats:sec>\n                  <jats:title>Key Points<\/jats:title>\n                  <jats:list list-type=\"bullet\">\n                    <jats:list-item>\n                      <jats:p>\n                        Acute buprenorphine exposure significantly depressed pulmonary ventilation rate (V\u0307\n                        <jats:sub>I<\/jats:sub>\n                        ) during eupnea and hypoxic hypercapnia (HH) in awake neonatal rats.\n                      <\/jats:p>\n                    <\/jats:list-item>\n                    <jats:list-item>\n                      <jats:p>\n                        Buprenorphine-induced hypoventilation was driven by reduced tidal volume (V\n                        <jats:sub>T<\/jats:sub>\n                        ) and breathing frequency.\n                      <\/jats:p>\n                    <\/jats:list-item>\n                    <jats:list-item>\n                      <jats:p>Buprenorphine also reduced oxygen consumption (V\u0307O\u2082) and carbon dioxide production (V\u0307CO\u2082).<\/jats:p>\n                    <\/jats:list-item>\n                    <jats:list-item>\n                      <jats:p>Naloxone given after buprenorphine failed to reverse hypoventilation.<\/jats:p>\n                    <\/jats:list-item>\n                    <jats:list-item>\n                      <jats:p>\n                        In contrast, pre-treatment with either naloxone hydrochloride or peripherally restricted naloxone methiodide mitigated buprenorphine-induced hypoventilation by preserving V\n                        <jats:sub>T<\/jats:sub>\n                        .\n                      <\/jats:p>\n                 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